PHYSIOLOGY OF TRANSITION PERIOD IN NEONATES WITH RESPECT TO RESPIRATORY SYSTEM

Speaker: Dr Bhagirath.S.N

Moderator: Dr Sarika

Prenatal development of the lungs

Some concepts….

Surface TensionProperty of the surface of a liquid that allows it to resist an external force. (by virtue of cohesive forces between its molecules)

What exactly does surfactant do..?It forms a monolayer that adheres closely to the alveolar interface and prevents the sac from collapsing once the fluid is removed..

How then is the fluid removed..?Most of it is expelled by the upper airways. Rest of it is drained by the lymphatics and capillaries.

What provides the force required to force open the partiallycollapsed fluid filled alveolar sacs..?A negative intrathoracic pressure of -30 to -70 cms of H2O that is created by the first gasp of air.

What induces this gasp of air..?Clamping of the cord asphyxiates the baby provoking a violent gasp of air.

Some concepts….(continued)

So, does this first gasp of air represent the first breath…? • Boddy & Robinson ((1971) were among the first to demonstrate foetal breathing in-utero.

• Patrick et al (1980) demonstrated the presence of fetal breathing >30% of the time in utero and further recorded a increase in movements subsequent to a maternal meal.

• Motoyama demonstrated a increase in FRC on inducing hypercapnia in the fetus.

So, the traditional concept that the first gasp represents the first breath now stands challenged.

Why does the fetus need to breathe when the placenta is breathing for it..?• Unclear. But thought to be as a prenatal practice for postnatal life and probably to act as a stimulus for lung development…

Respiratory rateO2 consumption is neonates is double that of an adult

Minute ventilation is very high

Minute ventilation is the product of respiratory rate and tidal volume

Since tidal volume is almost same as a child/adult on a volume/Kg/body weight measure, the only factor that can be augmented is the rate.

This explains why the respiratory rate is so high in a neonate.

Analogous to increasing heart rate to compensate for the fixed stroke volume, so that on the whole cardiac output remains maintained.

Respiratory reserveLung volume of the neonate is disproportionately small in relation to body size

Further complicated by the increased metabolic rate (O2 consumption/unit body weight being twice as that of adults)

i.e. the respiratory reserve is less

This calls for increased ventilatory requirements.

Relative to the increased ventilatory requirements the lung surface area available for gas exchange is less

Primary reason why neonates become rapidly desaturated with hypoventilation or apnea of relatively short duration

Implication

Compliance-ability of the lungs & thorax to expand

To not react is to be compliant; To react is to be less compliant;

What determines the recoiling nature of the lung & the chest wall..?

Elastic fibers in the lung tissue, elastic rib cage architecture, good diaphragmatic effort all of which are either deficient or immature in the neonate.

Neonatal lung

Adult lung

Compliance …(contd)

Neonates have a high compliance because:

• Poorly developed intercostal muscles

• Pliable rib cage (cartilaginous)

• Poor diaphragmatic effort due to abundance of type 2 fast twitch, low oxidative fibers that contract in quick succession but invariably fatigue early.

Anaesthetic implication

• Under general anesthesia the neonatal lungs are more prone to collapse as skeletal muscle relaxation ensues around the chest wall, what precious little rigidity that prevented the collapse is now lost.

Surfactant

• Secreted by type 2 pneumocytes

• Chemically: dipalmitoylphosphatidylcholine

• maintains distensibility of alveoli by reducing surface tension

• Laplace law: The gas pressure (P) needed to keep equilibrium between the collapsing force of surface tension (γ) and the expanding force of gas in an alveolus of radius r is expressed as P = 2 γ/r

• decreased levels are seen in premature babies and babies born to

diabetic mothers

• decreased levels predispose to respiratory distress syndrome (RDS) ,

which includes:1. Alveolar collapse2. Decreased compliance3. Hypoxia4. Increased work of breathing5. Ultimately respiratory failure.

• Treatment includes administration of exogenous surfactant

Control of breathing

• The respiratory centers are still immature and are unable to control

breathing effectively.

• Neonatal response to hypercapnia is less compared to a child but

none the less is mounted in the form of hyperventilation albeit for

short durations.

• Under conditions of hypothermia, initial hyperventilatory response

may be blunted.

• Periodic breathing

breathing is interposed with repetitive short apneic spells lasting 5

to 10 seconds without haemoglobin desaturation or cyanosis

Seen in both REM and NREM sleep.

thought to be due to changes in respiratory mechanics rather than

reduced sensitivity to CO2

Control of breathing….(Contd.)

•Apnea of prematurity & hypoxia

unexplained cessation of breathing for 15 seconds or longer or a

shorter respiratory pause associated with bradycardia (heart rate

<100), cyanosis, or pallor

may be related to an immature respiratory control mechanism

thought to be due to changes in respiratory mechanics rather than

reduced sensitivity to CO2

Persistent pulmonary hypertension of newborn• Collapsed fluid filled alveoli, collapsed capillaries and decreased perfusion offer resistance to flow of blood through pulmonary vasculature in utero

• i.e. pulmonary vascular resistance is high in utero

• If the same resistance due to any reason is encountered in the post natal period, then the pressure in the pulmonary artery is elevated to overcome such resistance.

• i.e. pulmonary artery hypertension ensues..

Precipitating factors include:1. Hypoxia2. Preterm3. Birth asphyxia4. Meconium aspiration5. Sepsis6. Congenital diaphragmatic hernia7. Maternal use of NSAIDs.

Persistent pulmonary hypertension of newborn….(Contd)Other risk factors include:1. Maternal diabetes2. Asthma3. Caesarean delivery

Increased pulmonary artery

pressure

Increased right ventricular pressure

Increased right atrial pressure

Throws open the foramen ovale

Blood reaches the aorta

as pulmonary artery pressure

is high

Ductus arteriosus is thrown

open

Hypoxia & normal to elevated

PaCO2

• Treatment Increase tissue oxygenationTarget PaO2 -50-70 mm of HgMechanical ventilationHigh frequency ventilationExogenous surfactantAlkalinisationECMOSildenafil

Persistent pulmonary hypertension of newborn….(Contd)•Meconium aspiration

this is different from meconium aspiration at labour

This happens in utero.

Seen when the fetus has been exposed to prolonged periods of

hypoxia

Can predispose to persistent pulmonary hypertension of newborn.

References….

Ganong’s review of physiology23rd editionP582, 584

Guyton & Hall’s Text book of Physiology

11th editionP1022, 1023

References….

Clinical Anesthesia by Paul.G.Barash6th editionP1127, 1129

Miller’s Anesthesia 7th Edition, Vol 1

P889. 890

References….

Physiology for anesthetistsWolters KluwerChapter 4

Smith’s anesthesia for infants and children

Motoyama and DavisChapter 6